Managing Nausea and Vomiting : Current Strategies

Kitty Garrett, Kayo Tsuruta, Shirley Walker, Sharon Jackson and Michelle Sweat
Crit Care Nurse 2003;23:31-50
2003 American Association of Critical-Care Nurses Published online http://www.cconline.org Personal use only. For copyright permission information: http://ccn.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECT

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Critical Care Nurse is the official peer-reviewed clinical journal of the American Association of Critical-Care Nurses, published bi-monthly by The InnoVision Group 101 Columbia, Aliso Viejo, CA 92656. Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949) 362-2049. Copyright 2003 by AACN. All rights reserved.

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CoverArticle

CE

Continuing Education

Managing Nausea and Vomiting

CURRENT STRATEGIES
Kitty Garrett, RN, MSN, CCRN Kayo Tsuruta, RN, MSN, AOCN Shirley Walker, RN, MSN Sharon Jackson, RN, MSN Michelle Sweat, RN, BSN

he topic of nausea and vomiting is all too familiar to most nurses. Nausea and vomiting are unpleasant complications or indications of many medical conditions and are adverse effects of hundreds of medications. Nausea and vomiting occur so frequently that they are almost considered acceptable, usually referred to as minor and considered more of an inconvenience or a nuisance than a medical problem. This duo, however, is not only unpleasant but can be debilitating and can cause unnecessarily prolonged recovery times and increased costs. In critically ill patients, severe or protracted nausea and vomiting can lead to serious complications such as aspiration pneumonia, dehy-

This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:

CE

1. Discuss the mechanisms of nausea and vomiting 2. Identify preoperative and postoperative factors that influence the development of nausea and vomiting 3. Describe treatment options for nausea and vomiting

Authors
Kitty Garrett is a critical care clinical nurse specialist at St. Joseph Hospital in Augusta, Ga. She has worked in critical care and has been CCRN certified for 20 years. Kayo Tsuruta has 7 years of nursing experience and is currently working as an oncology nurse at Athens Regional Medical Center in Athens, Ga. Shirley Walker is an instructor in the nursing staff development department at AnMed Health in Anderson, SC. She has 23 years of nursing experience. Sharon Jackson has 12 years of experience in medical-surgical nursing and emergency department nursing. She is a major in the US Army Nursing Corps and is stationed at Tripler Army Medical Center in Honolulu, Hawaii. Michelle Sweat is a senior staff nurse in the medical intensive care unit at the Medical College of Georgia Hospital in Augusta. She is currently enrolled in the critical care clinical nurse specialist program at the Medical College of Georgia School of Nursing.
To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 8092273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.

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dration, malnutrition, and disruption of the surgical site.1,2 Metabolic disturbances such as metabolic alkalosis, hyponatremia, hypochloremia, and hypokalemia may occur. Vomiting after craniotomy or any brain injury causes an increase in intracranial pressure. These complications can be life-threatening. Nausea and vomiting can also cause patients to experience increased anxiety and dissatisfaction with the hospital experience and can contribute to future anticipatory nausea.2 Also, the increased resources and time needed to treat a patient with nausea and vomiting can have a profound economic impact.2 Interest in this topic was recently renewed because of an enhanced understanding of the physiological mechanisms involved in the process of nausea and vomiting. Much has been published about nausea and vomiting as it relates to chemotherapy and postoperative nausea and vomiting, but many correlates can be drawn to critical care patients. In this article, we present current knowledge about the physiological mechanisms of nausea and vomiting and compare therapeutic agents (pharmacological and nonpharmacological) recommended for treating and preventing nausea and vomiting. Because it is now understood that most episodes of nausea and vomiting are preventable, implications for critical care nursing will focus on prevention rather than control of nausea and vomiting.

nomenon should be assessed separately. Nausea is defined as a subjectively unpleasant wavelike sensation in the back of the throat or epigastrium associated with pallor or flushing, tachycardia, and an awareness of the urge to vomit.1 Sweating, excess salivation, and a sensation of being cold or hot may occur. Vomiting, or emesis, is characterized by contraction of the abdominal muscles, descent of the diaphragm, and opening of the gastric cardia, resulting in forceful expulsion of stomach contents from the mouth.1 Retching involves spasmodic contractions of the diaphragm and the muscles of the thorax and abdominal wall without expulsion of gastric contents, the so-called dry heaves.1

Mechanisms of Nausea and Vomiting

The activation of a nucleus of neurons located in the medulla oblongata, known as the vomiting center, initiates the vomiting reflex. The vomiting center can be activated directly by signals from the cerebral cortex (anticipation, fear, memory), signals from sensory organs (disturbing sights, smells, pain), or signals from the vestibular apparatus of the inner ear (motion sickness). The vomiting center can also be activated indirectly by certain stimuli that activate the chemoreceptor trigger zone (CTZ)3 (Figure 1). The CTZ is located in the highly vascular area postrema on the surface of the brain. This area lacks a true blood-brain barrier and is exposed to both blood and cerebrospinal fluid; thus, the CTZ can react directly to substances in the blood.2 The CTZ can be activated by signals from the stomach and small intestine traveling along

vagal afferent nerves or by the direct action of emetogenic compounds that are carried in the blood (anticancer drugs, opioids, ipecac). Specific neurotransmitters and neuromodulators in the CTZ identify substances as potentially harmful and relay impulses to the vomiting center to initiate the vomiting cascade so that the harmful substance can be expelled. These neurotransmitters are serotonin, dopamine, acetylcholine (muscarinic cholinergic), and histamine. A fifth chemoreceptor, the neurokinin-1 neuropeptide, also called substance P, is currently under study.4,5 Stimulation of these chemoreceptors triggers activation of the vomiting center. Therefore, any interference with the transmission of these chemoreceptors prevents the vomiting center from being activated. Many antiemetics act by blocking 1 or more of these receptors.3 Dopamine antagonists block dopamine receptors; muscarinic antagonists block acetylcholine receptors; histamine blockers block histamine receptors; and serotonin receptor blockers block serotonin receptors. The adverse effects of these drugs are also determined by which receptor site is blocked3 (Table 1).

Chemotherapy-Induced Nausea and Vomiting

Nausea and vomiting are among the most distressing and debilitating adverse effects of chemotherapy. Even though chemotherapeutic agents are not routinely administered in critical care, cancer patients who have had chemotherapy are often admitted to critical care areas. Hence, a discussion of nausea and

Definitions
Nausea and vomiting are basic human protective reflexes against the absorption of toxins, as well as responses to certain stimuli.2 The terms nausea and vomiting are often used together, although each phe-

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Stomach and small intestine Sensory input Sight Smell Pain Vestibular apparatus

5HT DA

Blood-borne emetics Chemotherapy Opioids Ipecac

Health System Pharmacists (ASHP) recommends prophylactic antiemetic therapy when drugs with antiemetic potential of levels 2 to 5 are used1 (Table 2). Risk Factors In addition to the emetic potential of the chemotherapeutic agents, several other risk factors can be used to predict the likelihood of CINV. Patients younger than 50 years have more nausea and vomiting than do older patients.1 Women are more susceptible than men, presumably because of the influence of hormones.2 A history of motion sickness, pregnancy-related nausea and vomiting, or nausea and vomiting with previous chemotherapy are all positive predictors of CINV.1 Patients who use alcohol heavily or who have done so in the past have a reduced risk of emesis.1,11 Patterns of Nausea and Vomiting Anticipatory nausea and vomiting occur before the beginning of a new cycle of chemotherapy, in response to conditioned stimuli such as the smells, sights, and sounds of the treatment room or the presence of a specific person designated to administer the chemotherapy.12 Anticiatory nausea usually occurs 12 hours before administration of chemotherapy in patients who have experienced failed control of nausea and vomiting in previous treatments. Acute nausea and vomiting occur within the first 24 hours after the administration of chemotherapy, usually within the first 1 to 2 hours. This type is initiated by stimulation primarily of dopamine and serotonin receptors in the CTZ, which triggers the vomiting cascade.1 It resolves within 24 hours.

Higher centers Anticipation Fear Memory

ff

Vomiting center

Vomiting via output to stomach, diaphragm, and abdominal muscles

Figure 1 The emetic response: stimuli, pathways, and receptors.

CTZ indicates chemoreceptor trigger zone. Reprinted from Lehne et al,3 with permission.

vomiting would not be complete without a description of the clinical studies in this area. Mechanism Chemotherapeutic agents stimulate enterochromaffin cells in the gastrointestinal tract to release serotonin, which activates serotonin receptors. Activation of the receptors activates the vagal afferent pathway, which activates the vomiting center and causes an emetic response.10 The

Va

ga

CTZ

la

er

en

ts

5HT DA M

H1 M

Receptors: 5HT = Serotonin DA = Dopamine M = Muscarinic cholinergic H1 = Histamine1

emetic potential of a chemotherapeutic agent itself is the major stimulus for nausea and vomiting in chemotherapy-induced nausea and vomiting (CINV).1 Chemotherapeutic agents are rated according to their emetic potential; 1 indicates the least potential, and 5 indicates the greatest. An example of an agent with the lowest emetic potential (1) is vincristine. An example of an agent with the highest emetic potential (5) is cisplatin. The American Society of

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Table 1 Summary of antiemetic therapy as recommended by the American Society of Health System Pharmacists, the American
Site of action Drug type Examples Indications

Indirect stimulation of vomiting center through receptor sites (chemoreceptor trigger zone) Serotonin receptors Serotonin (5HT3) receptor antagonists Ondansetron (Zofran) First-line therapy for acute CINV and RINV: use on day of chemotherapy or radiation therapy only, not more than 24 hours later First-line therapy for prevention of PONV and treatment of breakthrough nausea and vomiting Opioid-induced nausea and vomiting6 Granisetron (Kytril) First-line therapy for prevention of acute CINV and RINV

Only effective in acute phase, not useful beyond 24 hours

Not approved for PONV, although clinical trials are under way Dolasetron (Anzemet) Prevention of CINV

Prevention and treatment of PONV

Dopamine receptors

Dopamine antagonists

Promethazine (Phenergan)

PONV Breakthrough nausea and vomiting in CINV Opioid-induced nausea and vomiting
6

Phenothiazines

Chlorpromazine (Thorazine) Prochlorperazine (Compazine)

Acceptable alternative to droperidol in the prevention and treatment of PONV Breakthrough nausea and vomiting Established nausea and vomiting in RINV Opioid-induced nausea and vomiting
6

Droperidol (Inapsine) Butyrophenones

Prevention and treatment of established PONV and breakthrough nausea and vomiting in CINV only in patients who do not respond to other drug8 Can be given in combination with serotonin receptor antagonists and steroids in patients at high risk for PONV

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Society of Clinical Oncology, and Mayo Clinic Clinical Practice Guidelines

Dosage* Most common adverse effects Comments

CINV prevention: 24 mg by mouth or 8 mg IV 30 min before chemotherapy PONV prevention: 4 mg IV over 2-5 min immediately before or 8 mg by mouth 1 hour before induction of anesthesia PONV treatment: 1-4 mg IV CINV prevention: 2 mg by mouth or 10 g/kg IV 30 min before chemotherapy In recent trials,4 1 mg as effective as 2 mg and 50% less expensive PONV prevention: 20-40 g/kg IV (in clinical trials) CINV prevention: 100-200 mg by mouth or 1.8 mg/kg IV 30 min before chemotherapy PONV prevention: 12.5 mg IV intraoperatively or 100 mg by mouth 1 hour before induction of anesthesia PONV treatment: 12.5 mg IV postoperatively PONV prevention: 25 mg by mouth 1 hour before or 12.5-25 mg IV immediately before induction of anesthesia PONV treatment: 10-25 mg by mouth every 4-6 hours as needed or 12.5-25 mg intramuscularly or IV every 4 hr as needed; 25-mg rectal suppository every 12 hours PONV treatment: 10-25 mg by mouth every 4-6 hours as needed; 25- or 100-mg rectal suppository PONV prevention: 5-15 mg by mouth 1 hour, 5-10 mg intramuscularly 1-2 hours, or 5-10 mg IV 15-30 min before induction of anesthesia PONV treatment: 5-15 mg by mouth or 5-10 mg intramuscularly or IV every 3-4 hours; 2.5-, 5-, 25-mg rectal suppository CINV treatment: 5-20 mg by mouth, intramuscularly, or IV every 6 hours, 25-mg rectal suppository every 12 hours PONV prevention: 0.625-1.25 mg IV SLOWLY 5 min before termination of anesthesia PONV treatment: 0.625-1.25 mg IV slowly as needed Maximum dose: 2.5 mg

Mild to moderate and transient; headache most common

Advantages: one-time dosing lasts 24 hours, no known drug interactions, broad safety profile, may be taken with or without food, nonsedating Should be administered with steroids to prevent delayed nausea and vomiting Oral doses recommended over IV doses because former are equally effective, less costly, and more convenient Disadvantages: Increased cost; all serotonin receptor antagonists equally effective at equivalent doses, so cost should be a factor in making a choice

IV dolasetron may cause changes in intervals on electrocardiograms; use with caution in prolonged conduction disorders

Not first-line drug in breakthrough CINV because of cost Not first-line drug in chronic opioid-induced nausea and vomiting because of cost; may be used as first-line drug in acute episodes of opioid-induced nausea and vomiting

Oversedation; lethargy, postural hypotension; skin sensitivity; dystonic reactions Extrapyramidal reactions or paradoxical reactions occur more commonly in children Widely used because they are inexpensive; moderately effective; available in IV, oral, and suppository forms Efficacy generally lower than efficacy of serotonin receptor antagonists Prochlorperazine more effective than promethazine for treating uncomplicated nausea and vomiting in patients in emergency department IV promethazine administered at a rate no greater than 25 mg/min IV prochlorperazine administered at a rate no greater than 5 mg/min Sedation, hypotension, tachycardia Prolonged QT interval leading to torsade de pointes Not available in oral form Should not be given to patients with long QT intervals Electrocardiographic monitoring should be done before administration and continued for 2-3 hours after treatment
7

Continued

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Table 1 Continued
Site of action Drug type Butyrophenones Examples Haloperidol (Haldol) Indications Primary PONV; breakthrough nausea and vomiting in CINV; opioidinduced nausea and vomiting; nausea and vomiting due to bowel obstruction Rescue therapy when serotonin receptor antagonists not 4 effective Metoclopramide (Reglan) Breakthrough nausea and vomiting in CINV; established nausea and vomiting in RINV Prevents nausea and vomiting by stimulating gastric emptying and blocking dopamine receptors Benzamide Opioid-induced nausea and vomiting6

Dopamine receptors Dopamine antago(continued) nists (continued)

Histaminic receptors

Antihistamines

Dimenhydrinate (Dramamine) Meclizine (Antivert)

Nausea and vomiting associated with motion sickness or vertigo

Muscarinic cholinergic receptors Neurokinin-1 receptors Other sites of action Mechanism unknown

Anticholinergics

Scopolamine

First-line drug in prophylaxis of nausea and vomiting associated with motion sickness CINV, sudden onset and delayed

Not yet available

Glucocorticoids

Dexamethasone (Decadron)

Drug of choice in prevention of delayed nausea and vomiting in CINV PONV with dolasetron

Methylprednisolone (Solu-Medrol) Cannabinoid Cannabinoids receptor sites (CB-1 and CB-2) exert central sympathomimetic action Limbic system inhibition Benzodiazipines Dronabinol (Marinol) Modestly effective in CINV; may be used in patients responding poorly to other antiemetics

Lorazepam (Ativan)

Used as adjunct, not primary drug, in anticipatory or delayed nausea and vomiting or breakthrough nausea and vomiting in CINV

*All dosages are from the American Society of Health System Pharmacists Clinical Practice Guidelines unless otherwise noted. CINV indicates chemotherapy-induced nausea and vomiting; IV, intravenously; PONV, postoperative nausea and vomiting; RINV, radiation-induced nausea and vomiting; SRA, serotonin receptor antagonist.

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Dosage* CINV treatment: 1-4 mg by mouth, intramuscularly, or IV every 6 hours

Most common adverse effects Nonsedating in lower doses; sedation, hypotension, tachycardia, extrapyrimidal effects similar to those of dopamine antagonists Sedation, restlessness, agitation, diarrhea, drowsiness, sleeplessness, dystonic reactions with higher doses

Comments Cost-effective alternative to serotonin receptor antagonists

CINV treatment: 2 mg/kg by mouth or IV every 2-4 hours for 2-5 doses for rescue therapy; for delayed nausea and vomiting, 0.5 mg/kg or 30 mg IV or by mouth every 4-6 hours for 3-5 days PONV prevention: 10-20 mg IV near the end of surgery PONV treatment: 10 mg IV over 1-2 min every 4-6 hours postoperatively

At high doses, also inhibits serotonin receptors Use no longer recommended by Mayo Clinic guidelines because of adverse effects of restlessness, agitation, and drowsiness Because of its ability to increase gastric and intestinal motility, contraindicated in patients with bowel obstruction, gastrointestinal hemorrhage, or perforation Slightly less effective than serotonin receptor antagonists and droperidol

Motion sickness and vertigo: 25-50 mg by mouth

Sedation, dry mouth, constipation, blurred vision

25-50 mg by mouth6 Motion sickness: patch 0.5 mg/24 hours every 3 days Dry mouth, drowsiness, impaired eye accommodation

Used as adjunct to prevent adverse effects in patients receiving dopamine receptor antagonists; use limited because dopamine receptors no longer first-line agents Patch applied behind ear 4 hours before travel; patch should last 3 days Investigational

CINV prevention: 20 mg by mouth or IV with serotonin receptor antagonists before chemotherapy CINV treatment: 10 mg by mouth or IV every 4-6 hours PONV prevention: 10 mg IV before induction of anesthesia9 CINV prevention: 40-125 mg 1-time dose before chemotherapy CINV treatment: 5-20 mg by mouth every 3-6 hours

Gastrointestinal upset, anxiety, insomnia, hyperglycemia

Used with serotonin receptor antagonists to enhance their benefit; yields increased protection Used alone for prevention of level 2 CINV Inexpensive Should be used with caution in patients with unstable diabetes mellitus

Drowsiness, dizziness, sedation, hypotension, vision difficulty, vasodilatation, euphoria, dysphoria (especially in older adults)

Other antiemetics more effective, but because the mechanism of action differs, cannabinoids may be given alone or in combination with other agents

CINV treatment: 1-2 mg by mouth, sublingually, intramuscularly, or IV every 6 hours

Sedation, amnesia, visual disturbances

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Table 2 Emetogenic potential of chemotherapeutic agents and standard treatments

Treatment Level* 5 (>90) Agent Cisplatin Cyclophosphamide (>1500 mg/m2) Carboplatin Cyclophosphamide (>750 mg/m2, <1500 mg/m2) Doxorubicin (>60 mg/m2) Methotrexate Doxorubicin Ifosfamide Irinotecan Cytarabine Docetaxel Etoposide 5-Fluorouracil Paclitaxel Bleomycin Fludarabine Vinblastine Vincristine Dexamethasone or methylprednisolone; prochlorperazine for adults Prevention Granisetron, ondansetron, or dolasetron with dexamethasone; or methylprednisolone Breakthrough Lorazepan, methylprednisolone, prochlorperazine, metoclopramide, dexamethasone, haloperidol, or dronabinol Delayed High-dose carboplatin: dexamethasone and metoclopramide or serotonin receptor antagonists High-dose carboplatin, cyclophosphamide, or doxorubicin: serotonin receptor antagonists and dexamethasone

4 (60-90)

3 (30-60)

For children Chlorpromazine, lorazepam, or methylprednisolone

For children Chlorpromazine, lorazepam, or serotonin receptor antagonists and dexamethasone or methylprednisolone

2 (10-30)

1 (<10)

No treatment

*Numbers in parentheses are percentages of patients who experience nausea and vomiting without effective treatment.

Delayed nausea and vomiting begin at least 24 hours after the administration of chemotherapy and may last up to 120 hours. Patients who experience acute CINV are more likely to also experience delayed emesis.12 The causative mechanism in delayed nausea and vomiting is not well defined, but the metabolites of the chemotherapeutic agents are thought to continue to affect the central nervous system and the gastrointestinal tract.1,13(p546-549) For example, cisplatin causes delayed nausea and vomiting, up to 48 to 72 hours after administration, in more than half of all patients who receive the drug.1 Other agents that cause delayed nausea and vomiting are high-dose carboplatin, cyclophosphamide, and doxorubicin. Breakthrough nausea and vomiting occur despite preventive therapy

and require additional therapy.1 Antiemetic treatment administered to patients who have not responded to prophylactic regimens is often referred to as rescue therapy.13 Treatment Prevention of Acute CINV. Antiemetic therapies have been compared in many clinical trials, especially since the advent of the relatively new class of drugs, the serotonin receptor antagonists (SRAs). Because chemotherapeutic agents initiate activation mainly of serotonin receptors, which leads to CINV, the SRAs are among the most effective drugs for prevention of CINV. These drugs have become the gold standard of antiemetic therapy,10 and they are recommended by the ASHP as the drugs of choice in patients receiving chemotherapeutic agents with emetic

potential of 3 to 5.1 The SRAs prevent emesis by blocking the emetic response early in the emetic pathway.10 They are given to patients before chemotherapy to prevent CINV. Because the SRAs have no effect on the histaminergic, dopaminergic, or cholinergic receptors, they can provide highly effective relief of nausea and vomiting without many of the adverse effects associated with traditional antiemetic agents. Adverse effects of the SRAs are generally mild to moderate and transient; headache is the most common.10 The SRAs used most often are ondansetron (Zofran), granisetron (Kytril), and dolasetron (Anzemet). Unfortunately, their high cost may prevent some patients from benefiting from these medications (Table 3). Because SRAs are similarly effective for controlling acute nausea and

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vomiting, the investigators in several comparative medical trials concluded that the least expensive SRA should be used initially.1,4,12 Also, oral SRAs are less expensive than parenteral SRAs and are as effective as the intravenous form.1,4,10,12 Wickam11 found that because the SRAs are not structurally identical, they may have differences in efficacy, and she recommends that if an SRA is ineffective, a second SRA should be given. With less toxic chemotherapeutic agents, combinations of other antiemetics may be effective. Dexamethasone and prochlorperazine are recommended for chemotherapeutic agents that have mild to moderate emetic potential.1 The combination of dexamethasone with metoclopramide, although less effective, may also be an option. Prevention of Delayed CINV. The SRAs alone are not useful in delayed nausea and vomiting. Complete protection from vomiting occurs more

often in patients who are given ondansetron plus dexamethasone.1 Therefore, dexamethasone is the drug of choice for prevention of delayed nausea and vomiting.1,4,9 It should be administered with SRAs before chemotherapy. Treatment of Breakthrough CINV. If a patient experiences CINV within 24 hours despite preventive antiemetic treatment, a combination of different classes of antiemetic drugs is given. This intervention is called rescue therapy. Drugs of choice for such rescue therapy include prochlorperazine, thiethylperazine, or metoclopramide with or without diphenhydramine, or lorazepam, haloperidol, or dronabinol.1,15 Dronabinol may be indicated in refractory CINV unresponsive to other classes of drugs. Even though the SRAs may also be effective, their superiority over traditional, less expensive agents has not been determined.1 The choice of agent should be based on patient-specific factors.1 All

patients receiving chemotherapy should have antiemetics available as needed for rescue from breakthrough nausea and vomiting.1 If CINV persists after the breakthrough treatment, these drugs should be given on a scheduled basis rather than on an asneeded basis. Treatment of Anticipatory CINV. Behavioral interventions are recommended for anticipatory emesis because they produce physiological relaxation, divert attention away from the conditioned stimulus and toward relaxing images, and enhance feelings of control.1 The amnestic and anxiolytic properties of lorazepam may also help prevent anticipatory nausea and vomiting by blocking the memory of emesis associated with chemotherapy.1,13 Lorazepam should be given the night before and the morning of chemotherapy.13,15 In summary, nausea and vomiting are no longer inevitable compli-

Table 3 Comparative costs of antiemetic agents

Agent Ondansetron (Zofran) Granisetron (Kytril) Dolasetron (Anzemet) Promethazine (Phenergan) Chlorpromazine (Thorazine) Prochlorperazine (Compazine) Droperidol (Inapsine) Haloperidol (Haldol) Metoclopramide (Reglan) Dimenhydrinate (Dramamine) Scopolamine (Transderm Sco p) Methylprednisolone (Solu-Medrol) Dronabinol (Marinol) Lorazepam (Ativan)
Data from Drug Topics Redbook.14

Mean wholesale price, $US Intravenous form 25.65 (2 mg/mL, 2-mL vial) 195.20 (1 mg/mL, 1-mL vial) 166.20 (20 mg/mL, 5-mL vial) 2.27 (25 mg/mL, 1-mL ampoule) 2.85 (50 mg/mL, 1-mL ampoule) 2.60 (25 mg/mL, 2-mL vial) 4.73 (10-mg ampoule) 5.71 (2.5 mg/mL, 2-mL ampoule) 4.59 (2.5 mg/mL, 1-mL ampoule) 8.15 (5 mg/mL, 1-mL ampoule) 4.56 (5 mg/mL, 2-mL vial) 9.42 (50 mg/mL, 1-mL vial) 2.38 (0.4 mg/mL, 1 mL) 3.51 (40-mg injection) 9.01 (125-mg injection) Not applicable 10.66 (2 mg/mL, 1-mL vial)

Oral form 27.80 (8-mg tablet) 16.69 (4-mg tablet) 47.05 (1-mg tablet) 55.31 (50-mg tablet) 73.31 (100-mg tablet) 0.04 (25-mg tablet) 0.06 (50-mg tablet) 0.62 (50-mg tablet) 0.54 (5-mg tablet) 0.81 (10-mg tablet) Not applicable 0.06 (5-mg tablet) 0.25 (10-mg tablet) 0.41 (20-mg tablet) 4.85 (patch) 0.48 (4-mg tablet) 8.06 (5-mg tablet) 0.67 (1-mg tablet) 0.99 (2-mg tablet)

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cations of chemotherapy; most patients can get complete control of these adverse effects. The drugs of choice for prevention of acute CINV are the SRAs. Recommended treatment for prevention of delayed CINV is dexamethasone. The drug of choice for anticipatory nausea and vomiting is lorazepam. Breakthrough nausea and vomiting can be treated with prochlorperazine, metoclopramide, haloperidol, or dronabinol (Table 1).

receiving anesthesia. Although significant progress has been made in preventing this type of nausea and vomiting, it still occurs in 20% to 30% of patients after surgery.1,2 Mechanism In postoperative nausea and vomiting, a wide range of stimuli contribute to the emetic response. Most anesthetic agents and opioids stimulate the vomiting center indirectly through the CTZ. Associated factors that directly stimulate the vomiting center include sensory input (visual, olfactory, and pain) and the vestibular apparatus. Nitrous oxide directly stimulates the gastrointestinal tract, which activates the vomiting center.2

Postoperative Nausea and Vomiting

The term acute postoperative nausea and vomiting is defined as any episode of nausea or vomiting that occurs within 24 hours of

Causes Preoperative Factors. The occurrence of postoperative nausea and vomiting is influenced by several factors.1,2,16 The risk is higher in adults than in children, in women than in men, and in patients with a history of motion sickness or previous postoperative nausea and vomiting.1 The prevalence is also greater in obese patients and in patients with delayed gastric emptying disorders such as gastroesophageal reflux disease, gastrointestinal obstruction, chronic cholecystitis, and neuromuscular disorders.1 A history of smoking is associated with a decrease in the likelihood of postoperative nausea and vomiting.16 Patients characteristics have a cumulative effect in influ-

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encing the prevalence of postoperative nausea and vomiting. Intraoperative Factors. The type of surgical procedure can also influence the occurrence of postoperative nausea and vomiting. The rate is high in patients undergoing laparoscopic procedures related to abdominal distention because of the carbon dioxide used for visualization.1,2 The prevalence of postoperative nausea and vomiting is also greater after plastic, ophthalmic, orthopedic shoulder, gynecologic, and ear, nose, and throat surgeries than after other procedures.1,2 Intubation itself can evoke nausea and vomiting. Longer procedures with general anesthesia are associated with more nausea and vomiting than are shorter procedures.1,2 The

type of anesthetic used is also a factor. General anesthetics vary in their propensity to cause postoperative nausea and vomiting. Etomidate, ketamine, nitrous oxide, and inhaled agents increase the risk of nausea and vomiting.1,2 Gastric distention caused by suction or vigorous positive pressure ventilation via face mask may also increase the risk of postoperative nausea and vomiting.1,2 Some medications used in association with anesthesia decrease the risk of postoperative nausea and vomiting. These include atropine, which has a vagolytic effect, and propofol (Diprivan).1 Although the exact mechanism of the antiemetic effect of propofol is not clear, the drug may have a weak serotonin antagonistic effect.9

Postoperative Factors. During the postoperative period, the 2 most common causes of nausea and vomiting are unrelieved pain (especially visceral or pelvic) and the opioids prescribed to control the pain. Adequate pain relief reduces the occurrence of nausea by 80%.2 Opioids stimulate nausea and vomiting by a direct action on the CTZ.2 Unrelieved pain directly stimulates the vomiting center (Figure 1). Nausea can also be precipitated by sudden motion, changes in body position, premature oral intake, and hypotension.1,2 Prevention If postoperative nausea and vomiting can be predicted, then they should be preventable. However,

Circle number 122 on Reader Service Card

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prevention is sometimes difficult because of the wide range of stimuli that contribute to the emetic response. Also, many of the pathways involved in the control of postoperative nausea and vomiting are complex and are not fully understood. The decision to provide antiemetic therapy should be based on a patients risk factors and potential for serious sequelae from vomiting. All patients at high risk should receive prophylactic antiemetics, preferably a combined regimen.9 Evidence is conflicting on whether all surgical patients should receive routine prophylactic antiemetics.1,2 Selection of an antiemetic should be based on safety and efficacy, the patients risk factors, the patients satisfaction, and cost. No single antiemetic is superior in every situation. For the prevention of postoperative nausea and vomiting, the ASHP guidelines recommend administration of droperidol (Inapsine) or an SRA.1 Droperidol, a dopamine receptor antagonist, is cost-effective and produces marked tranquilization and sedation. It allays apprehension and provides a state of mental detachment and indifference while maintaining a state of reflex alertness. However, since the ASHP guidelines were published, studies have indicat-

ed that droperidol can cause a prolonged QT interval, which can lead to potentially fatal cardiac dysrhythmias. The Food and Drug Administration now requires a blackbox warning, and therefore droperidol is no longer considered a first-line agent in postoperative nausea and vomiting.7 Ondansetron (Zofran) and dolasetron (Anzemet) are commonly used SRAs. Although granisetron (Kytril) prevents postoperative nausea and vomiting, it is not currently approved for this purpose. The cost of using SRAs is thought to be justified by patients satisfaction in avoiding postoperative nausea and vomiting. Dolasetron or ondansetron can be given preoperatively or intraoperatively as a single dose. Combination drugs (eg, dolasetron plus dexamethasone) increase efficacy, especially in highrisk patients. Administration of intravenous dexamethasone before induction of anesthesia prevents postoperative nausea and vomiting.9 The use of supplemental oxygen has been shown to decrease the occurrence of postoperative nausea and vomiting.17 Also, the restriction of oral intake until the return of bowel function after surgery has been used for decades to decrease the occurrence of postoperative nau-

sea and vomiting. Alternative antiemetic drugs include metoclopramide, chlorpromazine, prochlorperazine and promethazine. Treatment For established postoperative nausea and vomiting, the choices of antiemetic are almost identical to those used to prevent this type of nausea and vomiting, with a slight difference in some of the dosages. The SRAs are considered first-line agents, and the same alternative drugs are recommended as those used to prevent postoperative nausea and vomiting. Dopamine antagonists, because they are inexpensive, are often used. Unlike other sedatives used also for nausea and vomiting, propofol is currently indicated only for sedation. Because it has antiemetic properties, several studies have been done to evaluate subhypnotic doses in the treatment of postoperative nausea and vomiting. Those studies had conflicting outcomes. Fujii et al18 found that a small dose (0.5 mg/kg) was an effective antiemetic compared with droperidol and metoclopramide. Gan et al19 concluded that patient-controlled delivery of propofol decreased the prevalence of postoperative nausea and vomiting compared with placebo. Other studies20,21 in which propofol was used postoperatively indicated that propofol did not decrease the prevalence of postoperative nausea and vomiting. Pain medication should not be withheld because of its potential to cause nausea and vomiting.2 In patients who do not respond to initial therapy with 1 antiemetic agent, an agent from another pharmacolog-

Table 4 Frequent causes of nausea and vomiting in critical care

Surgery Unrelieved pain Pancreatitis Diabetic ketoacidosis Increased intracranial pressure Meningitis Heart failure Hepatobiliary causes Cerebrovascular accident Hypotension Bowel obstruction/ileus Drugs (opioids, antibiotics, drug overdose, nonsteroidal anti-inflammatory drugs, selective serotonin reuptake inhibitors, digitalis) Peritonitis Hyponatremia Brain tumors, vestibular involvement Myocardial infarction, especially inferior Anxiety Gastrointestinal bleeding Renal failure, uremia Hypercalcemia

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ical class should be added, the dose of the antiemetic should be increased to the maximum accepted range, or a combination of both approaches should be used.1 In patients sensitive to opioids, nonopioid analgesics such as ketorolac (Toradol) can be used as an alternative to control postoperative pain.2 Ketorolac is a nonsteroidal antiinflammatory drug and may cause gastrointestinal irritation and toxic effects on the kidneys. In summary, the SRAs are recommended as first-line agents in the prevention and treatment of postoperative nausea and vomiting. Administration of antiemetic medications is generally considered safe, despite an occasional adverse reaction.

Other Causes of Nausea

Many medications, medical conditions, and procedures can induce nausea and vomiting. Table 4 lists the causes most common in critical care. Drugs that cause gastric irritation (eg, nonsteroidal anti-inflammatory drugs, selective serotonin reuptake inhibitors, and antibiotics) can cause nausea. Examples of drugs that stimulate the vomiting center indirectly through the CTZ are digoxin, morphine, alcohol, ipecac, and anticancer drugs. Motion sickness and inner ear disorders cause nausea by directly stimulating the vomiting center. Nausea can also be induced by olfactory, visual, vestibular, and psychogenic stimuli2 (Figure 1). Opioids directly stimulate serotonin and dopamine receptors in the CTZ, which in turn stimulate the vomiting center. The analgesic effect of opioids is mediated by the activation of both 1 and 2 receptors.

Figure 2 A, The P6 point is located on the anterior side of the forearm bilaterally about 3 to 5 cm above the wrist between the tendon of the flexor carpi radialis and the palmaris longus. B, The ST36 point is located on the anterior side of the lower extremity bilaterally about 10 cm below the knee.

Activation of the 2 receptor unfortunately accounts for delayed transit time through the gastrointestinal tract, which contributes to nausea and vomiting. Currently, no opioid agonists can selectively activate specific receptors, and therefore nausea and vomiting remain adverse effects of opioid therapy.6 Tolerance to this opioid-induced nausea and vomiting usually occurs within days to weeks.6 Although the SRAs do relieve opioid-induced nausea, they are not considered first-line drugs in long-term therapy because of their

cost. Less expensive drugs such as phenothiazines, butyrophenones, anticholinergics, and motility agents are recommended.21 In the acute short-term, however, SRAs may be used as first-line agents for opioidinduced nausea and vomiting.

Pharmacological Management
The goal of pharmacological interventions is to prevent or minimize nausea and/or vomiting. Antiemetic agents are more effective at preventing emesis than at suppressing it.1,3 For prevention,

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antiemetics can be administered orally or parenterally.3 For suppression of ongoing emesis, oral therapy is ineffective; parenteral administration is required. Parenteral therapy includes intravenous, intramuscular, and rectal routes of administration. Nausea is a complex response. No single pharmacological agent is available that blocks all the receptors that trigger nausea or elicit vomiting. Also, adverse effects may limit the use of certain antiemetics. Therefore, the choice of drugs should be individualized to each patients needs. Combination antiemetic therapy using agents with different mechanisms of action may be necessary.1 Antiemetic therapies have been compared in multiple clinical trials. On the basis of the results, clinical practice guidelines for the prophylaxis and treatment of nausea and vomiting have been developed. These guidelines continue to be refined as more research is completed. Table 1 summarizes current pharmacological recommendations, emphasizing those from the ASHP,1 the American Society of Clinical Oncology,4 and the Mayo Clinic.8 Table 3 provides a cost comparison of antiemetic agents. The pharmacological recommendations presented in this article are intended for adults and not for children. Specifically, the dopamine antagonists such as prochlorperazine and metoclopramide should not be used in children. Data are insufficient to support the use of metoclopramide in children except to facilitate smallbowel intubation in endoscopic procedures. Children are more prone than adults to extrapyrimidal reactions or paradoxical reactions of rest-

lessness and excitement when given prochlorperazine.1

Nonpharmacological Management
Dietary Management The traditional dietary approach to postoperative management is to provide nothing by mouth and to use a nasogastric tube for gastric decompression to prevent nausea. Once bowel sounds resume, the tube is removed, a clear liquid diet is introduced, and the diet is gradually advanced as tolerated. Although this approach is commonly practiced, use of this regimen is not supported by published reports. Jeffrey et al22 challenged this traditional approach; they found no difference in postoperative nausea and vomiting in patients receiving a clear liquid diet compared with patients receiving a regular diet as the first postoperative meal. Other dietary modes of decreasing nausea are eating bland foods such as dry toast or crackers and drinking carbonated beverages such as ginger ale.2 Alternative/Complementary and Behavioral Therapy Although medications are the first-line treatment for nausea and vomiting, the use of alternative or complementary measures as adjuncts may improve patients outcomes and help reduce costs. Acupressure/Acupuncture. Acupressure originated in China. It is based on the principle of qi or chi, the energy present in living organisms. When the flow of qi is stagnant, the physical condition is affected. The application of pressure to specific points on the body unblocks abnormal energy flow and relieves signs

and symptoms. The 2 points that are effective in lessening nausea and vomiting are P6 and ST36 (Figure 2). Firm and steady pressure applied to these points with the fingers lessens the intensity of chemotherapy-induced nausea.23 Grealish et al24 reported that a 10-minute foot massage was effective in decreasing the intensity of pain and nausea and improving relaxation among cancer patients. Acupuncture also decreases nausea and vomiting; it is based on the same principles as acupressure.25 Because acupuncture requires trained and certified personnel, it may not be a cost-effective method of treatment. However, Medicare, Medicaid, and some third-party payers now cover acupuncture fees. A list of certified acupuncturists can be found by visiting the Web site of the American Academy of Medical Acupuncture at www.medicalacupuncture.org or that of the National Acupuncture and Oriental Medicine Alliance at www.acupuncturealliance.org. Transcutaneous Electrical Nerve Stimulation. Recently, a wristbandtype device for transcutaneous electrical nerve stimulation, the ReliefBand, was approved by the Food and Drug Administration as an over-the-counter device. It is also based on the principles of acupressure and is applied at the P6 acupressure point. Use of the ReliefBand has provided significant relief from nausea and vomiting among cancer patients.26,27 Relaxation. In relaxation training, patients are instructed to relax muscles in order to decrease the tension of the muscles. Patients should be encouraged to take slow deep breaths; the attention to breathing serves as a distraction. In postopera-

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tive nausea and vomiting, this technique also helps the body rid itself of any residual anesthetic agent.2 Imagery training involves using mental processes that increase relaxation, such as recalling pleasant memories and imaging positive thoughts. Relaxation and imagery can be used together or separately. Therapeutic touch can also be used as a comfort measure.2 These techniques are effective for treating nausea and vomiting, pain, and insomnia.28 Music. Ezzone et al29 concluded that music has a beneficial effect on nausea and vomiting. Music decreases the intensity of nausea and vomiting among cancer patients, when it is used with pharmacological antiemetic treatment.

Herbs. The use of herbs to treat nausea and vomiting is controversial. In one study,2 ginger root was more effective than placebo for treatment of postoperative nausea and vomiting. However, Ernest and Pittler30 reviewed 6 studies on the effect of ginger to treat nausea and vomiting and concluded that ginger may or may not be effective for postoperative nausea; ginger did appear to reduce the occurrence of nausea related to seasickness, morning sickness, and chemotherapy. Dried ginger in capsules has been used to treat car sickness in animals. Aromatherapy. The use of aromatherapy is also controversial because its scientific effectiveness and safety have not been estab-

lished. Tate31 studied the use of peppermint oil for postoperative nausea. Peppermint oil with a relatively high content of menthol was smelled by an experimental group of patients who underwent gynecologic surgery. Although the results were not statistically significant, the experimental group had a lower prevalence and/or intensity of nausea after surgery, less requirement for antiemetics, and more tolerance to analgesia, which usually causes nausea, than the control group did. Abdominal Implant. The Food and Drug Administration recently granted humanitarian device exemption approval for an implantable system (Enterra, Medtronic Inc, Minneapolis, Minn) for the treat-

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ment of chronic, intractable nausea and vomiting due to gastroparesis of diabetic or idiopathic origin. The device consists of 2 leads with electrodes that are implanted in the antrum of the stomach and connected to a pulse generator that is surgically placed in the lower part of the abdomen. The system is programmed to deliver low-frequency, low-amplitude electrical pulses continuously to the stomach muscle. Although the exact mechanism for the suppression of nausea is not known, it is thought that the effect is due to the neurostimulation of central vagal afferent nerve pathways, not by enhanced gastric emptying as previously thought (W. L. Starkebaum, Medtronic, Inc, oral

communication, November 7, 2001). The device is externally programmed in a fashion similar to that used with cardiac pacemakers.32

Implications for Critical Care Nursing

Critical care nurses are responsible for assessing the causes of nausea and vomiting, administering appropriate antiemetic agents, evaluating the effects of the agents, and providing information to physicians when changes in treatment are indicated. Antiemetic agents are most useful when given prophylactically; it is much easier to prevent signs and symptoms than to control them. Identification of patients at high risk for nausea and vomiting allows earli-

er intervention in the prophylaxis for and therefore the control of these effects. Even though anesthesiologists routinely screen patients preoperatively to determine which are high-risk patients, this information must be communicated to the critical care nurses caring for the patients in order to optimize patients care. It may be helpful to know, for example, that patients with a history of motion sickness may be more susceptible to movement-induced postoperative nausea and vomiting.2 Care can then be taken to ensure slow and smooth movements in transferring and turning a patient who has such a history. Consideration should be given to administering antiemetics on a

Circle number 128 on Reader Service Card

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scheduled basis, rather than as needed, for patients at high risk for postoperative nausea and vomiting.2 Causes and Assessment Patients should be assessed for pain, including postoperative pain, and should be treated promptly to prevent associated nausea and vomiting. Suspected opioid-induced nausea may be evaluated by determining the temporal relationship between the time the opioid was given and the onset of nausea.6

increased in a patient with acute coronary syndrome exacerbated by nausea and vomiting. The pulmonary system should be assessed for indications of pulmonary aspiration, especially in patients receiving tube feedings. Nosocomial pneumonia can be caused by aspiration of oropharyngeal secretions or gastric contents into the lungs. Preventive measures such as elevating the head of the bed, ensuring that bowel sounds are present, and routinely checking

Although medications are the first-line treatment for nausea and vomiting, the use of alternative or complementary measures . . . may improve patients outcomes. . .
A careful systems assessment should be done, with all possible causes investigated before nausea and vomiting are automatically labeled as opioid induced.6 The cardiovascular system should be assessed for hypotension due to hemodynamic compromise. Nausea may be the first symptom of hypotension. Hemodynamic sources (increased or decreased heart rate, decreased preload, increased afterload, or decreased contractility) should be investigated. Postoperatively, hypotension may be due to the restriction of fluids preoperatively, intraoperative blood loss, and the use of anesthetics, analgesics, and sedatives.2 Vagal maneuvers caused by retching and vomiting, as occur in inferior myocardial infarction, can cause bradycardia. Myocardial oxygen demand may be residual feeding volumes may help prevent pulmonary aspiration. The gastrointestinal system should be assessed for abdominal distention, organomegaly, and presence of bowel sounds. Signs of hypomotility may suggest an increased risk for nausea and vomiting. Postprandial nausea and vomiting associated with bloating and satiety suggest a gastrointestinal cause.6 Nausea and vomiting can be indications of as well as complications of acute pancreatitis. Nausea that occurs primarily with movement can be assumed to be generated by impulses from the vestibular center.6 Because strong odors can cause or exacerbate nausea and vomiting, especially postoperatively, exposure to odors from nearby food, strong perfume, and cleaning solutions should be minimized.2

Vomiting can also cause dehydration, leading to fluid and electrolyte imbalance. Fluid and electrolyte levels must be assessed and the fluids and electrolytes replaced accordingly. Nausea, headache, and oliguria are common indications of hyponatremia, which can cause cerebral edema and death if untreated. Hypercalcemia can cause nausea and vomiting. Hypokalemia and life-threatening dysrhythmias can result from loss of electrolytes due to vomiting. Neurological causes should also be considered. Increased intracranial pressure can cause refractory nausea, and some brain tumors cause vomiting without nausea. Nausea and vomiting cause an increase in intracranial pressure and can be life threatening in a patient with brain injury. Vomiting must be avoided in patients with suspected aneurysms in order to prevent subarachnoid hemorrhage. In patients with spinal cord trauma, the movements associated with vomiting can cause further injury to the spinal cord. Nausea and vomiting occur frequently after craniotomy. Antiemetic therapy may cause sedation, making postoperative neurological assessment difficult. Disruption of the surgical site during vomiting can cause excess bleeding, a possible need for return to surgery, increased morbidity, increased scarring, and prolonged recovery time. Such disruption can be especially dangerous after eye, neck, or facial surgery. The explosive pressure generated during vomiting can dislodge indwelling tubes or wires, particularly those that are strategically placed, such as drains used to diminish intracranial pressure, cardiac pacing wires, and chest tubes.

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Medications should be evaluated for their emetogenic potential. Common offenders are chemotherapeutic agents, opioids, nonsteroidal anti-inflammatory drugs, antibiotics, and selective serotonin reuptake inhibitors. Assessment of nausea and vomiting should include determination of the severity, duration, and number of episodes. A visual analog scale can be used to measure the severity of nausea, with a scale of 1 to 10, similar to that used as a pain scale.1,10 Prevention and Treatment The prevention and treatment of nausea and vomiting will become even more of a healthcare concern as hospitals are required to make the most efficient use of available resources, decrease the frequency of complications, and decrease patients lengths of stay.1 Traditional, convenient, cost-effective approaches to the prevention and treatment of nausea and vomiting in the intensive care unit include the use of nasogastric tubes for gastric decompression and the use of phenothiazines or metoclopramide as antiemetics. This regimen may still be effective for most patients. However, the lack of efficacy and the adverse effects (sedation, hypotension) of these drugs may limit their use. The most recently published Mayo Clinic guidelines no longer recommend metoclopramide because of the increased occurrence of restlessness, agitation, insomnia, and drowsiness associated with use of this drug.4 Also, patients may not respond to the initially prescribed therapy. If no response occurs, then an agent from another pharmacological class should be added, the

Case Study
S.W. is a 68-year-old man who was brought to the emergency department with a severe headache, nausea, and right-sided weakness. A computed tomogram of the head revealed a ruptured cerebral aneurysm that was then surgically repaired. He returned to the neurological intensive care unit with an external ventricular drain in place and an intracranial pressure measurement of 5 mm Hg. His vital signs, electrocardiographic rhythm, and oxygen saturation were stable. He has a history of colon cancer and had a right hemicolectomy 4 months ago. This surgery was followed by chemotherapy with 5-fluorouracil and leucovorin. His last chemotherapy was 1 week ago. He has had moderate to severe nausea and vomiting and has been taking ondansetron (Zofran) 8 mg by mouth twice a day at home. He also has been taking prochlorperazine (Compazine) 10 mg by mouth before each meal. Laboratory data indicate normal liver and kidney function. S.W. has nausea after his aneurysm surgery. Promethazine (Phenergan) 12.5 mg intravenously is ordered to be administered every 4 to 6 hours as needed. Questions 1. After S.W. receives 2 doses of promethazine, he is sleepy but still has persistent unrelieved nausea. Which of the following are appropriate actions for the critical care nurse to take? a. Give another dose of promethazine. b. Report to the physician that promethazine does not relieve the patients nausea and vomiting. c. Check the external ventricular drain to ensure proper functioning. d. Review the patients medication administration record to see if any medication may be contributing to his nausea and vomiting. e. Assess the patients serum level of sodium. 2. S.W. is receiving morphine intravenously as needed for pain. His oncologist was consulted for his uncontrolled nausea and vomiting. The oncologist ordered ondansetron on a scheduled basis, and prochlorperazine and lorazepam (Ativan) on an as-needed basis. What is the rationale for this order? a. Ondansetron is indicated in postoperative nausea and vomiting when other antiemetics are ineffective; it is imperative to keep the intracranial pressure controlled after craniotomy. b. Ondansetron can prevent opioid-induced nausea. c. Ondansetron is less sedating than promethazine; it will not mask the neurological assessment. d. Ondansetron is a serotonin receptor antagonist, which prevents stimulation of the vomiting center. Prochlorperazine blocks dopamine receptors in the chemoreceptor trigger zone and also inhibits stimulation (such as

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caused by odors and pain) to the vomiting center. Lorazepam is indicated in anticipatory nausea. 3. On the third postoperative day, S.W.s nausea and vomiting have been well controlled, and he can tolerate oral intake. However, he complains that he has nausea whenever a nurse brings a bag of intravenous solution into his room because it reminds him of his chemotherapy. Which antiemetic is the best choice for this type of nausea? a. prochlorperazine 10 mg by mouth b. ondansetron 8 mg by mouth c. lorazepam 1 mg by mouth d. promethazine 12.5 mg intravenously Answers 1. b, c, d, and e When an antiemetic is ineffective, other types of drugs should be considered. Other possible causes of nausea should be assessed. These include medical history of chemotherapy, postoperative condition, possible increased intracranial pressure, and use of opioids for pain management. Also, nausea can be a symptom of hyponatremia, which can increase cerebral edema. 2. a, b, c, and d After a craniotomy, it is important to prevent nausea and vomiting that could increase intracranial

pressure. Administration of antiemetics should therefore be scheduled, not strictly ordered on an as needed basis. Ondansetron is effective in opioid-induced nausea and will not cause sedation, which could mask the neurological assessment. Administration of prochlorperazine as needed will help in breakthrough nausea evoked by stimulation of the vomiting center directly. Lorazepam is effective for anticipatory nausea and vomiting. 3. c Lorazepam reduces anticipatory nausea. Oral antiemetics are just as effective and more cost-effective than are parenteral antiemetics. Ondansetron is expensive and should not be used indiscriminately.

dose of the antiemetic should be increased to the maximum within an acceptable range, or both.1,9 This adjustment may require expansion of the use of serotonin receptor antagonists in critical care. Published views are conflicting about how much patients satisfaction should influence the choice of agent and override the cost concerns. If a drug is more expensive but it prevents complications and decreases length of stay, it would seem to be worth the extra cost in the final analysis. More studies on the economics are needed to help weigh the cost-benefit issue. Understanding the pathophysiology of nausea and vomiting will allow critical care nurses to assist in making appropriate decisions to prevent and treat these responses. Nonpharmacological methods should be considered as complementary therapy. Complete control, defined as no nausea or vomiting, should be the goal for every patient.
Acknowledgments
Parts of this article were previously published as a synopsis in the Oncology Nursing Society Critical Care Special Interest Group Newsletter, Vol 10, Issue 2, August 2001. We thank Dr Cynthia Chernecky, our faculty and mentor, for her inspiration, guidance, and support in writing this article. We appreciate the comments of our manuscript reviewers, as well as suggestions from Dr Mark Stewart, anesthesiologist, Dr Sandra Counts and Michael Madden, clinical pharmacists, and Dr Cynthia Chernecky, professor and oncology clinician. We also thank Shogo Tsuruta for his expert computer skills in compiling our pharmacology table.

References
1. ASHP therapeutic guidelines on the pharmacological management of nausea and vomiting in adult and pediatric patients receiving chemotherapy or radiation therapy or undergoing surgery. Am J Health Syst Pharm. 1999;56:729-764. Also available at: www.ashp.org/bestpractices. Accessed December 3, 2002. 2. Thompson HJ. The management of postoperative nausea and vomiting. J Adv Nurs. 1999;29:1130-1136. 3. Lehne RA, Moore LA, Crosby LJ, Hamilton DB. Pharmacology for Nursing Care. 3rd ed. Philadelphia, Pa: WB Saunders; 1998:794-798.

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4. Loprinzi CL, Alberts SR, Christensen BJ, et al. History of the development of antiemetic guidelines at Mayo Clinic Rochester. Mayo Clin Proc. 2000;75:303-309. 5. Bleiberg H. A new class of antiemetics: the NK-1 receptor antagonists. Curr Opin Oncol. 2000;12:284-288. 6. OMahony S, Coyle N, Payne R. Current management of opioid-related side effects. Oncology. 2001;15:61-77. 7. Ernst AA, Weiss SJ, Park S, Takakuwa KM, Diercks DB. Prochlorperazine versus promethazine for uncomplicated nausea and vomiting in the emergency department: a randomized double blind clinical trial. Ann Emerg Med. 2000;36:89-94. 8. US Food and Drug Administration. Medwatch: Summary of safety-related drug labeling changes approved by FDA Center for Drug Evaluation and Research: inapsine. November 2001. Available at: www.fda.gov/ medwatch/SAFETY/2001/nov01.htm. Accessed December 3, 2002. 9. Wang JJ, Ho ST, Tzeng JI, Tang CS. The effect of timing of dexamethasone administration on its efficacy as a prophylactic antiemetic for postoperative nausea and vomiting. Anesth Analg. 2000;91:136-139. 10. Bremerkamp M. Mechanism of action of 5HT3 receptor antagonists: clinical overview and nursing implications. Clin J Oncol Nurs. 2000;4:201-207. 11. Wickam RS. Ondansetron Versus Granisetron: Control of Nausea & Emesis, Satisfaction, and Quality of Life [dissertation]. Chicago, Ill: University of Illinois at Chicago; 1999. 12. Gralla RJ, Osoba D, Kris MG, et al. Recommendations for the use of antiemetics: evidence-based clinical practice guidelines. J Clin Oncol. 1999;17:2971-2994. Also available at: asco.org. Accessed December 3, 2002. 13. Yarbro CH, Frogge MH, Goodman M, Groenwald SL. Cancer Nursing: Principles and Practice. 5th ed. Boston, Mass: Jones & Bartlett; 2000. 14. Drug Topics Redbook. Montvale, NJ: Medical Economics, Thomson Healthcare; 2001. 15. American Cancer Society, National Comprehensive Cancer Network. Nausea and Vomiting: Treatment Guidelines for Patients with Cancer. Atlanta, Ga: American Cancer Society; 2001. 16. Sinclair DR, Chung F, Mezei G. Can postoperative nausea and vomiting be predicted? Anesthesiology. 1999;91:109-118. 17. Greif R, Laciny S, Rapf B, Hickle RS, Sessler DI. Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Anesthesiology. 1999;91:1246-1252. 18. Fujii Y, Tanaka H, Toyooka H. Preoperative oral granisetron prevents PONV. Acta Anaesth Scand. 1998;42:653-657. 19. Gan TJ, El-Molem H, Ray J, Glass PS. Patient controlled antiemesis: a randomized, double-blind comparison of two doses of propofol versus placebo. Anesthesiology. 1999;90:1564-1570. 20. Bree SE, West MJ, Taylor, PA, Kestin IG. Combining propofol with morphine in patient-controlled analgesia to prevent postoperative nausea and vomiting. Br J Anaesth. 1998;80:152-154. 21. Montgomery JE, Sutherland CJ, Kestin IG, Sneyd JR. Infusions of subhypnotic doses of propofol for the prevention of postoperative nausea and vomiting. Anaesthesia. 1996;51:1073-1074.

22. Jeffrey KM, Harkins B, Cresci GA, Martindale RG. The clear liquid diet is no longer necessary in the routine postoperative management of surgical patients. Am Surg. 1996;62:167-171. 23. Dibble SL, Chapman J, Mack KA, Shin, AS. Acupressure for nausea: results of a pilot study. Oncol Nurs Forum. 2000;27:41-47. 24. Grealish L, Lomasney A, Whiteman B. Foot massage: a nursing intervention to modify the distressing symptoms of pain and nausea in patients hospitalized with cancer. Cancer Nurs. 2000;23:237-243. 25. Somri M, Vaida SJ, Sabo E, Yassain G, Gankin I, Gaitini LA. Acupuncture versus ondansetron in the prevention of postoperative vomiting: a study of children undergoing dental surgery. Anaesthesia. 2001;56: 927-932. 26. Pearl ML, Fischer M, McCauley DL, Valea FA, Chalas E. Transcutaneous electrical nerve stimulation as an adjunct for controlling chemotherapy-induced nausea and vomiting in gynecologic oncology patients. Cancer Nurs. 1999;22:307-311. 27. Woodside Biomedical. Woodside Biomedical received FDA clearance to market Reliefband device over-the-counter to consumers [New Products]. Clin Nurse Specialist. 2000;14:150. 28. Fleet SV. Relaxation and imagery for symptom management: improving patient assessment and individualizing treatment. Oncol Nurs Forum. 2000;27:501-510. 29. Ezzone S, Baker C, Rosselet R, Terepka E. Music as an adjunct to antiemetic therapy. Oncol Nurs Forum. 1998;25:1151-1156. 30. Ernest E, Pittler MH. Efficacy of ginger for nausea and vomiting: a systematic review of randomized clinical trials. Br J Anaesth. 2000;84:367-371. 31. Tate S. Peppermint oil: a treatment for postoperative nausea. J Adv Nurs. 997;26:543-549. 32. Henney JE. Implant for chronic nausea [letter]. JAMA. 2000;283:2779.

patients undergoing ambulatory laparoscopic cholecystectomy. Am J Surg. 2000;179:60-62. Mickle J. The use of haloperidol to treat nausea. Oncol Nurs Forum. 1998;25:1309. Potter KL, Schafer SL. Nausea and vomiting. Am J Nurs. April 1999;99(suppl):2-4, 34-36. Souney PE. Treatment of severe nausea and vomiting: an evidence-based approach. Am J Gastroenterol. 2000;95:2121-2122. Watson S, Benson J, Joy J. Marijuana and medicine: assessing the science base: a summary of the 1999 Institute of Medicine Report. Arch Gen Psychiatry. 2000;57:547-552. Zarate E, Watcha MF, White PF, Klein KW, SaRego M, Stewart DG. A comparison of the costs of efficacy of ondansetron versus dolasetron for antiemetic prophylaxis. Anesth Analg. 2000;90:1352-1358.

Bibliography
Anastasia PJ. Effectiveness of oral 5-HT3 receptor antagonists for emetogenic chemotherapy. Oncol Nurs Forum. 2000;27:483-493. Epstein O, Perkin GD, deBonon DP, Cookson J. Clinical Exam. 2nd ed. St Louis, Mo: Mosby Times Mirror; 1997:185. Fabling JM, Gan TJ, El-Moalen HE, Warner DS, Borel CO. A randomized, double blinded comparison of ondansetron, droperidol, and placebo for prevention of postoperative nausea and vomiting after supratentorial craniotomy. Anesth Analg. 2000;91:358-361. Faries J. Controlling pain: controlling postoperative nausea. Nursing. August 1998;28:78. Gralla RJ, Navari RM, Hesketh PJ, et al. Singledose oral granisetron has equivalent antiemetic efficacy to intravenous ondansetron for highly emetogenic cisplatin-based chemotherapy. J Clin Oncol. 1998;16:1568-1573. Granisetron (Kytril tablets) [package insert]. Philadelphia, Pa: SmithKline Beecham; 1998. Hill RP, Lubarsky DA, Phillips-Bute B, et al. Cost-effectiveness of prophylactic antiemetic therapy with ondansetron, droperidol or placebo. Anesthesiology. 2000;92:958-967. Lieberman MA. Ondansetron versus placebo for prophylaxis of nausea and vomiting in

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CE
CE Test Instructions

Continuing Education

To receive CE credit for this test (ID C031), mark your answers on the form below, complete the enrollment information, and submit it with the $11 processing fee (payable in US funds) to the American Association of Critical-Care Nurses (AACN). Answer forms must be postmarked by February 1, 2005. Within 3 to 4 weeks of AACN receiving your test form, you will receive an AACN CE certificate.
This continuing education program is provided by AACN, which is accredited as a provider of continuing education in nursing by the American Nurses Credentialing Centers Commission on Accreditation. AACN has been approved as a provider of continuing education by the State Boards of Nursing of Alabama (#ABNP0062), California (01036), Florida (#FBN2464), Iowa (#332), Louisiana (#ABN12), and Nevada. AACN programming meets the standards for most other states requiring mandatory continuing education credit for relicensure.

CE Test Form Managing Nausea and Vomiting: Current Strategies

Objectives:

Test ID: C031 Test writer: Ruth Kleinpell-Nowell, RN, PhD, CS, CCNS Form expires: February 1, 2005 Contact hours: 1.5 Passing score: 9 correct (75%) Category: A Test fee: $11

1. Discuss the mechanisms of nausea and vomiting 2. Identify preoperative and postoperative factors that influence the development of nausea and vomiting 3. Describe treatment options for nausea and vomiting Mark your answers clearly in the appropriate box. There is only 1 correct answer. You may photocopy this form.

1. a 2. a 3. a 4. a b b b b c c c c d d d d

5. a 6. a b b c c d d

7. a b c d

8. a 9. a 10. a 11. a 12. a b b b b b c c c c c d d d d d

Name

Program evaluation
Objective 1 was met Objective 2 was met Objective 3 was met The content was appropriate My expectations were met This method of CE is effective for this content

Agree

Neutral

Disagree

Address City Phone ( ) State ZIP

E-mail address AACN member number

The level of difficulty of this test was: easy medium difficult To complete this program, it took me hours / minutes.

I would like to receive my certificate via e-mail (check box)

Mail this entire page to AACN, 101 Columbia, Aliso Viejo, CA 92656, (800) 899-2226

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CE Test Questions
Managing Nausea and Vomiting: Current Strategies

1.

Where is the vomiting center located? a. Hypothalamus b. Caudate nucleus c. Medulla oblongata d. Cerebellum Which of the following is not a neurotransmitter that can relay impulses to the vomiting center? a. Serotonin b. Dopamine c. Histamine d. Neurotensin Which antagonist blocks acetylcholine receptors? a. Dopamine b. Muscarinic c. Histamine d. Serotonin What emetic potential rating of chemotherapeutic agents indicates the least potential? a. 0 b. 1 c. 5 d. 10 What is an example of a chemotherapeutic agent with the highest emetic potential? a. Cisplatin b. Vincristine c. Carboplatin d. Doxorubicin Which of the following chemotherapeutic agents is not associated with delayed nausea? a. Cisplatin b. Vincristine c. Carboplatin d. Cyclophosphamide

7.

2.

Serotonin receptor antagonists are the drugs of choice in patients receiving chemotherapeutic agents with what emetic potential? a. 0 to 1 b. 1 to 2 c. 2 to 4 d. 3 to 5 Which antiemetic agent is indicated in refractory chemotherapy-induced nausea and vomiting unresponsive to other classes of agents? a. Ondansetron b. Granisetron c. Dolasetron d. Dronabinol Postoperative nausea and vomiting occurs in what percentage of patients after surgery? a. 10% to 20% b. 20% t0 30% c. 30% to 40% d. 40% to 50%

8.

3.

9.

4.

5.

10. Which of the following medications is associated with increased risk of nausea and vomiting? a. Atropine b. Propofol c. Ketamine d. Droperidol 11. Which of the following is associated with decreased occurrence of postoperative nausea and vomiting? a. Opioid use b. Supplemental oxygen c. Positive pressure ventilation d. General anesthesia 12. How much does adequate pain relief reduce the occurrence of nausea? a. 20% b. 40% c. 60% d. 80%

6.

52 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

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